AB1432 THE ASSOCIATION OF PAINFUL AND NON-PAINFUL COMORBIDITIES WITH CENTRAL MECHANISMS OF KNEE PAIN
Authors: H. R. Lewis, W. J. Chaplin, D. F. Mcwilliams, B. S. Millar, S. Shahtaheri, J. F. R. Gladman, D. Walsh
Journal: Annals of the Rheumatic Diseases (2022)

Background Central mechanisms of knee pain occur in the central nervous system and may intensify and prolong pain. Central pain mechanisms might be facilitated by ongoing nociceptive input. A link between multimorbidity and central mechanisms of knee pain is proposed; ongoing sensory inputs due to comorbidities may trigger changes in pain processing by the CNS. This might be particularly expected with painful comorbidities. Objectives To investigate potential relationships of painful and non-painful multimorbidity with central mechanisms of knee pain. Methods Cross-sectional analysis of self-report data from participants of the Investigating Musculoskeletal Health and Wellbeing cohort, who reported knee as their most bothersome site of joint pain over the previous month, with pain rated ≥1/10, and who had completed FRAIL and CAP-Knee (1) questionnaires. Two indirect measures suggesting central mechanisms involvement in knee pain were used as dependent variables; pain intensity (0-10 numerical rating scale) and CAP-Knee score (0-16 scale). Comorbidities were assigned either “painful comorbidity” or “non-painful comorbidity” status based on IASP classification of chronic pain criteria (2). Multivariable linear regression models, adjusted for age and sex, were employed to explore associations of comorbidity counts with pain intensity and CAP-Knee score. Results 736 participants satisfied inclusion criteria. 55% were female, mean age 71 (range 40 to 95). Painful comorbidity count and non-painful comorbidity count each had positive associations with pain intensity (β=0.42, 95% CI=0.29 to 0.54, p&lt;0.001; and β=0.31, 95%CI=0.16 to 0.45, p&lt;0.001, respectively). Painful and non-painful comorbidity counts each also were associated with CAP-Knee score (β=0.80, 95% CI=0.59 to 1.01, p&lt;0.001; and β=0.52, 95% CI=0.27 to 0.77, p&lt;0.001, respectively). Painful and non-painful comorbidity counts each remained significantly associated both with pain intensity and with CAP-Knee scores when both types of comorbidity count were included in the same multivariable model. Conclusion Both painful and non-painful comorbidities were positively associated with central mechanisms of knee pain, providing further insight into the interconnectedness of pain processing systems and the rest of the body. The explanation behind these relationships may depend on more than just ongoing nociceptive input. Future work should address possible contributions from genetic, pathophysiological, psychological, and pharmacological factors associated with comorbid diagnosis. References [1]Akin-Akinyosoye K, Frowd N, Marshall L, Stocks J, Fernandes GS, Valdes A, et al. Traits associated with central pain augmentation in the Knee Pain In the Community (KPIC) cohort. Pain [Internet]. 2018 Jun PMC5959005]; 159(6):[1035-44 pp.]. Available from: https://dx.doi.org/10.1097%2Fj.pain.0000000000001183 . [2]IASP-Task-Force-on-Taxonomy. Classification of Chronic Pain (Second Edition) [E-Book]. Seattle: IASP Task Force on Taxonomy. IASP Press; 1994 [Part I: Topics and Codes]. Available from: https://www.iasp-pain.org/publications/free-ebooks/classification-of-chronic-pain-second-edition-revised/ [date accessed: October 22, 2021]. Disclosure of Interests Harrison R. Lewis: None declared, Wendy J. Chaplin: None declared, Daniel F. McWilliams Grant/research support from: Receives grants and research support from Pfizer and Eli Lilly., Bonnie S. Millar: None declared, Seyed Shahtaheri: None declared, John F.R. Gladman: None declared, David Walsh Grant/research support from: Grants and research support were received from Pfizer and Eli Lilly.